期刊
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
卷 291, 期 6, 页码 G999-G1004出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.00187.2006
关键词
gastric adenocarcinoma; spasmolytic polypeptide expressing metaplasia; trefoil factor 2; intestinal metaplasia
资金
- NCI NIH HHS [1-P50-CA-95103] Funding Source: Medline
Gastric cancer in humans arises in the setting of oxyntic atrophy (parietal cell loss) and attendant hyperplastic and metaplastic lineage changes within the gastric mucosa. Helicobacter infection in mice and humans leads to spasmolytic polypeptide-expressing metaplasia (SPEM). In a number of mouse models, SPEM arises after oxyntic atrophy. In mice treated with the parietal cell toxic protonophore DMP-777, SPEM appears to arise from the transdifferentiation of chief cells. These results support the concept that intrinsic mucosal influences regulate and modulate the appearance of gastric metaplasia even in the absence of significant inflammation, whereas chronic inflammation is required for the further neoplastic transition.
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